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本文对14例HBV标志阳性的肝癌患者骨髓小粒的超微结构进行研究,结果发现:(1)红细胞、白细胞和巨核细胞三个系统的病态造血同时发生,可能是由于造血母细胞作为HBV的靶细胞受到攻击所致。(2) 细胞膜的畸形性变,反应了造血基质pH和细胞膜所带电荷的改变。白细胞膜的变化则可能与HBV对细胞膜的损伤有关。(3) 细胞核的退行性变化。说明胞核DNA合成障碍,可能与HBV DNA的侵害有关。(4) 病态血细胞在骨髓内崩解破坏,并可被功能活跃的细胞吞噬,形成无效血细胞生成的骨髓内循环,造成原位溶血。(5) 病态造血损伤了造血微环境,而造血微环境的变化,又影响造血母细胞的分化,二者相互作用,加重了病态造血的发展。(6) 发现骨髓内脂肪细胞具有吞噬功能并在薄的胞质中形成包函体。(7) 从肝癌患者临床血液学变化和病态造血的联系来看,肝癌患者临床血液学的变化机理在于骨髓的无效性血细胞生成的病态造血。
In this paper, 14 cases of HBV-positive liver cancer patients with bone marrow granulosa ultrastructure was studied and found that: (1) erythrocyte, leukocyte and megakaryocyte morbid hematopoiesis of the three systems simultaneously, probably due to hematopoietic progenitor cells as a target of HBV Cells are attacked. (2) The degeneration of the cell membrane changes, reflecting the changes in the pH of the hematopoietic matrix and the charge on the cell membrane. The changes of leukocyte membrane may be related to the damage of HBV to the cell membrane. (3) degeneration of the nucleus. Explain the nuclear DNA synthesis barriers, may be related to HBV DNA damage. (4) diseased blood cells in the bone marrow collapse and destruction, and can be phagocytosed by the function of active cells, the formation of inefficient hematopoietic bone marrow circulation, resulting in situ hemolysis. (5) Morbid hematopoietic damage hematopoietic microenvironment, and hematopoietic microenvironment changes, but also affect the differentiation of hematopoietic progenitor cells, the interaction between the two, aggravate the development of pathological hematopoiesis. (6) It was found that adipocytes in bone marrow have phagocytic function and form inclusion bodies in the thin cytoplasm. (7) From the clinical hematological changes in patients with liver cancer and pathological hematopoietic connection point of view, the mechanism of clinical hematology in patients with liver cancer is the ineffective bone marrow hematopoietic hematopoiesis.